Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
www.elsevier.com/locate/neubiorev
Review
Blindsight in action: what can the different sub-types of blindsight
tell us about the control of visually guided actions?
James Danckerta,*, Yves Rossettib,c,d
a
Department of Psychology, University of Waterloo, 200 University Avenue West, Waterloo, Ont., Canada N2L 3G1
Espace et Action, INSERM Unité 534 and Université Claude Bernard, 16 Avenue doyen Lépine, 69676 Bron Cedex, France
c
Service de Rééducation Neurologique, Hôpital Henry Gabrielle, Université Claude Bernard and Hospices Civils de Lyon,
Route de Vourles, St Genis Laval Cedex, France
d
Institut Fédératif des neurosciences de Lyon, 59 Boulevard Pinel, 69003 Lyon, France
b
Received 27 July 2004; revised 13 December 2004; accepted 7 February 2005
Abstract
Blindsight broadly refers to the paradoxical neurological condition where patients with a visual field defect due to a cortical lesion
nevertheless demonstrate implicit residual visual sensitivity within their field cut. The aim of this paper is twofold. First, through a selective
review of the blindsight literature we propose a new taxonomy for the subtypes of residual abilities described in blindsight. Those patients
able to accurately act upon blind field stimuli (e.g. by pointing or saccading towards them) are classified as having ‘action-blindsight’, those
whose residual functions can be said to rely to some extent upon attentive processing of blind field stimuli are classified as demonstrating
‘attention-blindsight’, while finally, patients who have somewhat accurate perceptual judgements for blind field stimuli despite a complete
lack of any conscious percept, are classified as having ‘agnosopsia’—literally meaning ‘not knowing what one sees’. We also address the
possible neurological substrates of these residual sensory processes. Our second aim was to investigate the most striking subtype of
blindsight, action-blindsight. We review the data relevant to this subtype and the hypotheses proposed to account for it, before speculating on
how action-blindsight may inform our normal models of visuomotor control.
q 2005 Elsevier Ltd. All rights reserved.
Keywords: Blindsight; Visuomotor control; Parietal cortex
Contents
1.
2.
3.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
A new taxonomy for residual behaviours in blindsight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1. Parietal cortex and action-blindsight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2. Action-blindsight operates in the here and now . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3. ‘Action-blindsight’ and the automatic pilot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Conclusion: action-blindsight—the automatic pilot in slow motion? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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1. Introduction
* Corresponding author. Tel.: C1 519 888 4567x7014; fax: C1 519 734
8631.
E-mail addresses: [email protected] (J. Danckert),
[email protected] (J. Danckert), [email protected]
(Y. Rossetti).
0149-7634/$ - see front matter q 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.neubiorev.2005.02.001
Blindsight refers to the residual visual abilities that some
patients with visual field defects demonstrate for stimuli
placed in their blind fields (Pöppel et al., 1973; Weiskrantz
et al., 1974; Perenin and Jeannerod, 1975). That is, although
patients with primary occipital (area V1) lesions are
essentially blind in one visual hemifield, they can
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J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
nevertheless demonstrate above chance performance when
responding to stimuli placed in their blind field. For example,
when asked to guess, under the appropriate conditions, the
location of a target that was briefly illuminated in the blind
hemifield, some patients guess the location accurately on
greater than 50% of trials (Weiskrantz et al., 1974; Zihl and
Werth, 1984a,b). Initially, the most common residual ability
demonstrated by blindsight patients was the ability to
localize, either by pointing or eye movements, targets
presented to the blind field. This ability to localize blind
field targets has also been demonstrated in hemidecorticated
patients (Perenin and Jeannerod, 1978; Ptito et al., 1991).
Taken together, these results suggest subcortical involvement in the residual functions of these patients (see
Jeannerod and Rossetti (1993) and Rossetti and Pisella
(2002) for review). However, since the earliest work on
blindsight, a wide range of residual functions have been
described, ranging from motion, form and wavelength
discrimination, to remarkable demonstrations of semantic
priming from words presented to the blind field (Danckert
et al., 1998; Magnussen and Mathiesen, 1989; Marcel, 1998;
Morland et al., 1999; Stoerig and Cowey, 1989). Although
still somewhat controversial, the performance of blindsight
patients suggests that visual information is able to reach
extrastriate visual cortex via pathways that do not depend on
processing in area V1 (see Stoerig and Cowey (1997) for
review). That is, it has been suggested that the residual
pathway which runs from the eye directly to the superior
colliculus and from there to the pulvinar nucleus of the
thalamus is responsible for the ability to localize blind field
targets (Weiskrantz et al., 1974; Zihl and Werth, 1984a,b).
The many and varied residual abilities demonstrated by some
blindsight patients may suggest, however, that blindsight
relies on not one, but many residual pathways (Danckert and
Goodale, 2000).1 Accordingly, visual projections from
subcortical structures, and in particular from the pulvinar,
may project not only onto parietal but also onto temporal
cortex. In addition, there is some recent anatomical evidence
from the macaque monkey that demonstrated direct koniocellular inputs from the interlaminar layers of the LGN to the
middle temporal (MT) motion-sensitive region of visual
cortex (Sincich et al., 2004). This finding provides evidence
for an alternate residual pathway that may subserve the
Riddoch phenomenon (see below for a more detailed
description of Riddoch phenomenon; Zeki and Ffytche
(1998); see also Benevento and Yoshida (1981) for
discussion of other LGN inputs to prestriate cortex).
1
There has been substantial debate in the literature concerning the
possibility that the residual abilities observed in blindsight patients are in
fact subserved by spared islands of cortex within V1. Recent neuroimaging
evidence demonstrating extrastriate activation in GY in the absence of any
such spared islands would seem to suggest this explanation does not suffice
for all patients (see Danckert and Goodale (2000) for discussion of this
issue).
In this selective review we will suggest a new taxonomy
for describing the various residual capacities demonstrated
by blindsight patients. It is important to note that this
taxonomy is intended to describe distinct types of residual
behaviours demonstrated by blindsight patients. While
some discussion of the neural networks underlying these
distinct behaviours is obviously warranted, at this stage such
a discussion is necessarily speculative. We will then explore
in more detail one of the proposed definitions of a blindsight
capability—namely ‘action-blindsight’ in which patients
with V1 lesions are able to localize blind field targets by
virtue of motor actions (e.g. pointing, grasping or saccades).
Finally, we will examine how action-blindsight can inform
models of visually guided action.
2. A new taxonomy for residual behaviours in blindsight
The earliest demonstrations of blindsight involved asking
the patient to motorically guess the location of a target that
had been briefly flashed in the blind field (Pöppel et al., 1973;
Weiskrantz et al., 1974; Perenin and Jeannerod, 1975).
Weiskrantz first coined the term ‘blindsight’ to account for
the paradoxical observation of accurate eye and arm
movements directed toward a visual target that was not
consciously perceived. Since these early demonstrations,
localization of targets presented to the blind field by various
means has been by far the most common residual ability
demonstrated (e.g. Weiskrantz et al., 1974; Perenin and
Jeannerod, 1975; Zihl and Werth, 1984a,b; Danckert et al.,
2003; Kentridge et al., 1999a,b). The ability to point or
saccade towards a blind field target strongly supported the
notion that the extrageniculate pathway directly from the eye
to the superior colliculus was responsible for this residual
ability (sometimes referred to as the retino-tectal pathway;
Fig. 1). This was especially true for saccades made to blind
field targets given the wealth of literature demonstrating
collicular involvement in the control of eye movements (see
Gaymard and Pierrot-Deseillingy (1999) for review). This
hypothesis gained even further support from findings in
hemidecorticated patients (Perenin and Jeannerod, 1978;
Ptito et al., 1991). That is, despite having little or no
remaining cortex in the damaged hemisphere, these patients
were nevertheless able to show above chance localization of
blind field targets, heavily implicating the retinofugal
pathway from the eye to the superior colliculus (Perenin
and Jeannerod, 1978; Ptito et al., 1991). The requirement that
an action—pointing or saccading—be used to demonstrate
above chance localization of blind field targets leads us to call
this kind of residual function ‘action-blindsight’.
As distinct from action-blindsight, some patients demonstrate residual abilities that do not completely lack a
conscious percept (Magnussen and Mathiesen, 1989;
Morland et al., 1999). For example, some patients may be
able to discriminate the direction of motion of a stimulus
presented in their blind field and furthermore, will report
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
1037
pulvinar
nucleus
optic chiasm
lateral
geniculate
nucleus
optic nerve
optic tract
lateral
geniculate
nucleus
superior
colliculi
optic radiations
extrastriate
visual cortex
primary visual
cortex (V1)
Primary geniculo-striate pathway
retina
optic
tract
LGNd
optic
tract
SC
V1
Retino-tectal pathway
retina
pulvinar
extrastriate cortex
Geniculo-extrastriate pathway
retina
optic
tract
interlaminar layers
(koniocellular) of LGN
extrastriate cortex
Fig. 1. Schematic representation of the various pathways for visual information from the retina to striate (V1) and extrastriate cortex. The primary
geniculostriate pathway is indicated by the by the dashed line from the temporal hemretina of the left eye and the widely space dotted line from the nasal
portion of the right eye. The two secondary pathways indicated are shown originating from the optic tract for clarity, with the retino-tectal pathway indicated by
the dashed/dotted line and the geniculostriate pathway indicated by the closely spaced dotted line. The pathways are also represented in simple box and arrow
form below the schematic. Note, that recent anatomical work in the monkey has shown direct koniocellular projections to area MT (Sincich et al., 2004). The
possibility exists for other such pathways from the interlaminar layers of the LGN to regions of extrastriate cortex other than area MT.
experiencing a sensation of that stimulus—albeit a sensation
that is qualitatively distinct from actual vision of the
stimulus. That is, the patient reports that they do not see, but
rather have a ‘sense’ or ‘feeling’ that something had moved
within their blind field, indicating some level of awareness
of that stimulus—the so-called Riddoch phenomenon
(Morland et al., 1999; Zeki and Ffytche, 1998). This kind
of residual ability in blindsight (awareness without seeing)
may be related to alerting functions and may also depend on
the integrity of the human homologue of monkey are MT
(sometime referred to as area V5), which is known to
subserve the processing of visual motion (e.g. see Dukelow
et al. (2001)). Given that recent fMRI research in humans
has demonstrated increased activation in some areas of the
human MT complex for both contralateral and ipsilateral
motion stimuli (Dukelow et al., 2001) it may even be
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J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
Table 1
A new taxonomy for residual behaviours demonstrated in blindsight
Action-blindsight
Attention-blindsight
Agnosopsia
Grasping, pointing, saccades
Covert spatial orienting, inhibition of return,
motion detection and discrimination
Forced-choice guessing, implicit processing
paradigms
SC—pulvinar—extrastriate visual cortex
(MT and dorsal stream)
Wavelength and form discrimination, semantic priming
Forced-choice guessing
Residual
behaviours
Paradigms
Direct behaviour towards blind field stimuli
Residual neural
pathways
SC—pulvinar—posterior parietal cortex
(dorsal stream)
Examples from
the literature
Danckert et al. (2003), Jackson (1999), Perenin
and Rossetti (1996), Weiskrantz et al. (1974),
Zihl and Werth (1984a,b) and Perenin and
Jeannerod (1975, 1978)
Danziger et al. (1997), Kentridge et al. (1999a,b),
Magnussen and Mathiesen (1989), Morland et al.
(1999) and Walker et al. (2000)
the case that this residual ability is supported, at least in part,
by the undamaged hemisphere. Further research would be
needed to explore this possibility, as well as examining in
more detail the contribution of subcortical structures. In
addition to motion discrimination, other residual abilities
have been demonstrated in blindsight that differ from those
described for action-blindsight. These include some aspects
of covert spatial orienting including inhibition of return and
implicit task interference effects (e.g. the flanker task with
flankers presented to the blind field) (Danckert et al., 1998;
Kentridge et al., 1999a,b; Danziger et al., 1997; Walker
et al., 2000). These abilities also appear to rely on
attentional processes and are not necessarily associated
with a specific action or effector. We refer to these residual
abilities as ‘attention-blindsight’ as a means of distinguishing them from ‘action-blindsight’. It is important to note
that attention and action-blindsight are closely related and
may depend upon aspects of the same residual neural
pathways. For example, intact covert orienting abilities in
blindsight patients may rely on the pathway from the eye to
the superior colliculus described above (Danziger et al.,
1997) as being responsible for ‘action-blindsight’. As we
will suggest later, the differences in action and attentionblindsight may lie in the regions of extrastriate visual cortex
involved. That is, it may turn out that the behavioural
distinction proposed here also reflects subtle differences in
the terminal region of extrastriate cortex that the residual
neural pathways responsible for those functions project to.
Furthermore, it may be the case that to demonstrate ‘actionblindsight’ the patient may also need attentional processes
of the type described in ‘attention-blindsight’ to be
functioning. An important determinant of the presence of
attention- or action-blindsight may be the nature of the task
used to examine residual functioning. Obviously, actionblindsight requires the patient to perform some kind of
action towards blind field stimuli whereas attention blindsight can be demonstrated using implicit processing
paradigms such as the flanker task in which the effect of
blind field stimuli on sighted field stimuli is the critical
measure (e.g. Danckert et al. (1998); Table 1). Research
employing both kinds of tasks within the same patients will
Interlaminar layers of the
dLGN—extrastriate visual
cortex (ventral stream)
Marcel (1998), Stoerig and
Cowey (1989) and Zeki and
Ffytche (1998)
be needed to determine the extent to which attention- and
action-blindsight co-exist or co-vary.
Finally, residual abilities such as form or wavelength
discrimination are more perceptual in nature and may rely on
very different residual pathways, perhaps from the interlaminar layers of the LGN and from there to regions of
extrastriate cortex that subserve the various functions
demonstrated (Jeannerod and Rossetti, 1993; Rossetti and
Pisella, 2002; Stoerig and Cowey, 1989, 1997; Danckert and
Goodale, 2000; Girard et al., 1992; Perenin and Rossetti,
1996; Rossetti, 1998; Stoerig, 1996). We refer to this kind of
blindsight as ‘agnosopsia’, a term first used by Zeki and
Ffytche (1998) which literally means ‘to not know what one
sees’ (Zeki and Ffytche, 1998)—that is, although the patient
is completely unaware of blind field stimuli, they can
nevertheless guess the correct perceptual characteristic at
above chance levels (Table 1). We would suggest that the
residual capacities falling under this classification depend on
very distinct residual neural pathways from those underlying
either attention- or action-blindsight. This may be evident at
the level of thalamic nuclei such that the pulvinar nucleus is
implicated in attention- and action-blindsight while the
interlaminar layers of the LGN may be implicated in
agnosopsia (Fig. 1 and Table 1). The latter pathway has
recently been shown to exist in the macaque and to maintain
direct connections with MT (Sincich et al., 2004). It remains
to be seen whether or not there are similar projections from
the interlaminar layers of the LGN to other regions
of extrastriate cortex. In addition, the projections to
extrastriate cortex from these residual pathways are also
likely to differ such that the projections for agnosopsia may
terminate in ventral extrastriate cortex known to be
responsible for form and colour perception, while the
projections for action-blindsight are more likely to terminate
in dorsal extrastriate and posterior parietal cortices known to
be important for the control of visually guided actions2
2
The final pathway for attention-blindsight is less clear. While residual
capacities such as motion discrimination may terminate in area MT
(importantly, this region is not generally considered to be either dorsal or
ventral in the human) other implicit processing capacities may terminate in
distinct regions of extrastriate cortex.
2.1. Parietal cortex and action-blindsight
Although the description of ‘action-blindsight’ discussed
above suggests involvement of the superior colliculus in the
ability to localize blind field targets, this explanation may not
be sufficient to explain the same ability when the required
response was not an eye movement but a pointing movement.
Indeed, Weiskrantz and colleagues (1974) found that in one
patient the ability to localize blind field targets was
dramatically better when the patient was required to point
to those targets rather than making an eye movement (Fig. 2).
Such a performance suggests cortical involvement in the
residual ability to localize blind field targets—a point made
by Weiskrantz and colleagues in their original work.
This is not to suggest that the superior colliculus is not
involved in the control of reaching movements (note, we are
using the term reaching here rather than pointing). Recent
work in the cat has demonstrated that stimulation of the
superior colliculus just after the onset of a reaching
movement leads to a perturbation in movement trajectory
(Courjon et al., 2004). Importantly, the perturbed reaching
movements are then corrected on-line such that the target of
the movement is still accurately acquired (Courjon et al.,
2004). In addition, the latency of saccades in the rhesus
monkey are reduced when they are accompanied by an arm
movement in the same direction as the saccade (Snyder et al.,
2002), suggesting a role for the superior colliculus in hand–
eye co-ordination (see Lunenburger et al. (2001) for review).
While this work demonstrates a role for the colliculus in the
transport component of reaching movements it does not
necessarily implicate the midbrain in the end stage
3
Stoerig (1996) discusses the different residual abilities related to lesions
at different levels in the visual system (e.g. from the optic nerve to the LGN
and through to V1). The distinction we are making here is within the final
residual pathway Stoerig discusses—the “extra-geniculo-striate pathways
and extrastriate cortical areas” (p. 402).
35
Eye movements
Finger position (degrees)
(Danckert and Goodale, 2000; Milner and Goodale, 1995).
Finally, the distinction between attention-blindsight and
agnosopsia is reminiscent of Weiskrantz’s Type I and Type II
blindsight distinction (Weiskrantz, 1998). That is, having a
‘sense’ of something in the blind field despite not ‘seeing’ it
per se—Weiskrantz’s Type II blindsight—is what characterises some of the phenomenon we are including under
attention-blindsight (e.g. Riddoch phenomenon; see Zeki
and Ffytche (1998)). In contrast, Type I blindsight is more
akin to agnosopsia in which the patient’s above chance
performance is never accompanied by a conscious percept
(albeit a degraded one; see Table 1). Our distinction focuses
on the behaviours demonstrated and to some extent the
methodologies used to elucidate those behaviours, rather
than the direct association between the behaviour and various
levels of awareness. What is important to emphasise here is
that different residual abilities in blindsight are likely to rely
on different residual neural pathways.3
Eye position (degrees)
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
30
25
20
15
10
5
0
5 10 15 20 25 30 35
Target position (degrees)
1039
90
Hand movements
75
60
45
30
15
0
15 30 45 60 75 90
Target position (degrees)
Fig. 2. Eye position (left panel) and finger pointing position (right panel) for
one blindsight patient (DB) tested by Weiskrantz and colleagues (1974).
The patient was required to localize blind field targets in both cases. Bars
represent the range of responses recorded at each target eccentricity. (Note:
the left panel is adapted from Fig. 2 of Weiskrantz et al. (1974) in which the
patient made saccades following the presentation of targets subtending 28 of
visual angle, while the right panel is adapted from Fig. 3b of Weiskrantz
et al. (1974) in which the patient pointed to targets subtending 28 7 0 of
visual angle).
components of pointing or grasping movements. Recent
work in the macaque monkey suggests that complex coding
of eye in head position may depend on structures downstream
from the colliculus (Klier et al., 2003). Results of this kind do
seem to suggest that complex components of visually guided
movements—over and above specification of direction and
amplitude—may depend on processing in neural regions
beyond the colliculus. What is important to emphasise here,
is that the residual pathway from the eye to the colliculus may
not fully account for residual abilities such as pointing to
blind field targets. Instead, additional processing in the
cortical regions within which this pathway terminates may be
required for accurate ‘action-blindsight’ to occur.4
Interestingly, pointing is not the only action that has
been shown to be above chance in patients with blindsight. More recently the ability of two blindsight patients
to process both size and orientation of a target presented
in the blind field was investigated using three types of
response: perceptual matching, goal directed action (i.e.
grasping to examine action-discrimination of size differences and posting a card to assess action-discrimination of
orientation differences; see Perenin and Vighetto (1988)
for original description of these tasks) and verbal report
(Perenin and Rossetti, 1996; Rossetti, 1998). They found
that the patient’s performance was above chance only
for the goal-directed actions (i.e. grasping or posting).
4
Presumably, hemidecorticate patients who are capable of localising
blind field targets at above chance levels are relying on only collicular and
subcortical processing to perform this task. There is some controversy
concerning the ability of such patients to localize blind field targets when
the target is of lower luminance than the background (King et al., 1996;
Scharli et al., 1999). The variable performance of hemidecorticate patients
under such conditions suggests that light scatter from high luminance
targets may actually be informing their performance. In addition, to our
knowledge there has been no study examining more complex residual
abilities such as grasping or wavelength discrimination in these patients.
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J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
That is, their patient was able to scale his grip aperture
(i.e. the distance between forefinger and thumb) appropriately to the target’s size but performed below chance
when perceptually matching the target’s size or verbally
reporting it. A similar performance was observed for
orientation judgements in the posting task. That is, the
patient performed above chance levels when required to
post an object through a slot that varied in orientation
from trial to trial, but performed at or below chance level
when matching or verbally reporting the slot’s orientation
(Perenin and Rossetti, 1996; Rossetti and Pisella (2002)).
Similarly, Jackson (1999) examined the ability of
patient GY, a well studied blindsight patient, to grasp
objects that extended into his blind field (the objects in
Perenin and Rossetti’s (1996) study were completely
within the blind field). That is, GY was asked to grasp
objects whose horizontal aspect covered the same extent
within his sighted field from trial to trial but extended into
his blind field to differing degrees. As was the case for the
patient in the Perenin and Rossetti (1996) study, GY was
able to demonstrate accurate grip scaling under these
conditions, such that the distance between his forefinger
and thumb was accurately scaled to the object size despite
the fact that he was unable to see the degree to which
objects extended into his blind field (Jackson, 1999). It
has also been demonstrated that the ability to accurately
scale grip aperture to blind field objects is lost when there
is a short delay between target presentation and the onset
of the movement into the blind field (note: this distinction
was based on the patient’s own movement initiation time,
such that movements with slower RTs showed a poorer
relationship to object size than did movements with faster
RTs; Rossetti, 1998). This result highlighted the importance of ‘on-line’ or automatic motor control in this
patient’s performance (Rossetti and Pisella, 2002). The
on-line control of such grasping movements has been
shown to depend on the dorsal ‘action’ pathway, which
runs from V1 through to posterior parietal cortex
(Jeannerod and Rossetti, 1993; Milner and Goodale,
1995; Goodale and Milner, 1992). While subcortical
structures such as the superior colliculus are also likely
to play a role in such movements, it is important to
emphasise that grip scaling and orientation judgements
require some degree of cortical involvement (Culham
et al., 2003). This is especially so for orientation
judgements as there have been no demonstrations to the
best of our knowledge of orientation selectivity in the
monkey superior colliculus. Therefore, for a blindsight
patient to demonstrate accurate grip scaling and orientation judgements towards blind field stimuli it is
necessary for visual information to reach the dorsal
extrastriate and posterior parietal cortex even in the face
of no input from V1. However, the input signals to this
area may arise from several different regions (Rossetti and
Pisella, 2002). As a matter of fact, patients with occipital
lesions exhibit poorer performance in the card posting
task described above (Perenin and Rossetti, 1996) than
do patients with a lesion of the ventral stream
(Goodale and Milner, 1992). A comparison of the two
types of performance is shown in Rossetti and Pisella
(2002), p. 70, Fig. 4.2). Therefore, the optimal processing
performed in the posterior parietal cortex is likely to
require inputs from both V1 and subcortical structures.
We recently demonstrated that an intact posterior
parietal cortex (PPC) is indeed necessary for demonstrating action-blindsight (Danckert et al., 2003). We explored
the ability of two patients with hemianopia to localize
blind field targets by pointing. In one patient (JR), the
PPC was generally spared, while in the other (YP) there
was more extensive damage of extrastriate cortex extending well into the PPC. On a touch screen version of the
pointing task only patient JR demonstrated above chance
localization. We then explored the kinematics of pointing
movements made to blind field targets (this unavoidably
led to significant changes in stimulus setup and target
types; Danckert et al., 2003). Although patient YP now
demonstrated above chance localization of blind field
targets, his performance showed several qualitative
differences when compared with patient JR. That is, the
strength of the relationship between actual target locations
and the patients’ responses was strongest for patient JR
in which there was greater sparing of extrastriate and
posterior parietal cortex. In addition, a strong relationship
was found between peak velocity, time to reach peak
velocity and target location only for patient JR (i.e. both
peak velocity and time to reach peak increased with
increasing target distance from fixation—a common effect
observed in healthy individuals; Danckert et al., 2003).
What this work clearly demonstrates is that an intact PPC
(and perhaps a greater degree of sparing of dorsal
extrastriate cortex) is needed for action-blindsight to be
apparent in patients with hemianopia—an assertion
initially made by Weiskrantz and colleagues (1974). Put
another way, for action-blindsight to be evident in a
hemianopic patient, the residual neural pathway implicated is likely to terminate in the dorsal ‘action’ stream
given the nature of the residual functions observed. This
pathway is ideally placed to subserve the residual abilities
we are calling ‘action-blindsight’ as it terminates in
regions of dorsal extrastriate cortex which in turn project
to the PPC—areas known to be crucial for the control of
eye and hand movements (Jeannerod and Rossetti, 1993;
Milner and Goodale, 1995; Culham et al., 2003; Connolly
et al., 2000).
Recent functional magnetic resonance imaging (fMRI) in
patient GY revealed activation in dorsal extrastriate cortex
in the damaged hemisphere in response to visual stimuli
placed in the blind field (Baseler et al., 1999). Similar
residual activity in dorsal stream structures has been
observed in monkeys following cooling of area V1 (Girard
et al., 1992, 1991). Interestingly no activity was found in the
ventral stream in spite of the anatomical connectivity
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
mentioned above. These results provide strong support
for the suggestion that action-blindsight depends on
the integrity of residual pathways that terminate in the
dorsal ‘action’ stream.
2.2. Action-blindsight operates in the here and now
The nature of the tasks used to explore residual visual
functions in blindsight may determine to a large extent the
performance of the patient (Danckert and Goodale, 2000;
Stoerig, 1996). For example, the discrimination of wavelength and form (i.e. what we and others have termed
agnosopsia; Zeki and Ffytche, 1998) is typically only
demonstrated in forced choice ‘guessing’ paradigms and
over a very large number of trials (Table 1; Stoerig and
Cowey, 1989). The residual abilities characteristic of
attention-blindsight (e.g. implicit interference effects,
motion discrimination) can be demonstrated using both
forced choice and implicit processing paradigms.5 In
contrast, action-blindsight for both pointing (or saccades)
and grasping movements, is typically demonstrated using
tasks in which the patients’ behaviour is directly measured
as they perform the action in their blind field (although this
is not always true, as localization of blind field targets has
also been explored using forced choice procedures; e.g.
Danziger et al. (1997)). Furthermore, significant demonstrations of action-blindsight have been observed after a
relatively small number of trials (Danckert et al., 2003;
Danziger et al., 1997; Perenin and Rossetti, 1996). Finally,
when a brief delay is introduced between the presentation of
the target in the blind field and the initiation of the action
directed towards that target, performance returns to chance
level (Rossetti, 1998).6 Taken together, this evidence
suggests that for action-blindsight to be evident the
behaviour must be performed in direct response to or
immediately after the presentation of a target.
The suggestion that action-blindsight operates only for
immediate actions fits nicely with work in healthy
individuals demonstrating both qualitative and quantitative
differences in the control of skilled actions performed
immediately in response to a target or following a delay
between target presentation and action onset (for review see
Rossetti and Pisella (2002) and Rossetti (1998)).
One elegant example of the effects of a delay on the control
of actions can be seen when healthy individuals are required
to grasp objects embedded within pictorial illusions
(e.g. size-contrast illusions including the Ebbinghaus and
Müller-Lyer illusions) (Aglioti et al., 1995; Gentilucci et al.,
1996). Typically, when subjects reach to grasp target objects
imbedded within a size-contrast illusion, no effect is seen
5
Of course for motion discrimination based on actual, albeit degraded
percepts, overt discriminations can be made (Morland et al., 1999).
6
Interestingly, the same effect of delay has been reported for the
somatosensory equivalent of blindsight—that is, ‘numbsense’ for both
tactile and proprioceptive stimuli (Rossetti et al., 1995).
1041
on grip scaling. In other words, the action is unaffected by
the illusion.7 In contrast, when asked to delay their action
for a period of 2 s or more, grip scaling now shows a
dramatic influence of the illusory context (Hu et al., 1999;
Hu and Goodale, 2000; see also Gentilucci et al. (1996)).
Interestingly, while the visual form agnosic patient DF is
able to accurately grasp objects (despite impaired perceptual
discrimination abilities with respect to those same objects),
when she performs the same actions following a delay
imposed between target presentation and movement onset,
her performance is now greatly impaired (Goodale et al.,
1991, 1994). Milner and Goodale (1995) suggested that the
differences in the immediate control of actions compared
with the control of the same actions following a delay, is
indicative of the division of labour between the dorsal
‘action’ and ventral ‘perception’ pathways. That is, while
the dorsal pathway, which runs from V1 to posterior parietal
cortex depends on moment-to-moment, or ‘on-line’ calculations of spatial relationships to control skilled actions,
the ventral ‘perception’ pathway, which runs from V1 to
inferotemporal cortex, operates on stable visual representations of objects and their spatial relationship to one
another stored in long term memory (see Rossetti and
Pisella (2002), Rossetti (1998), Pisella and Rossetti (2000)
and Milner and Dijkerman (in press) for review). If actionblindsight also depends on the dorsal pathway, then it too
should operate on a moment-to-moment basis. In other
words, action-blindsight should only be evident when the
patient initiates their action in immediate response to the
presentation of a target (obviously while maintaining central
fixation; see Danckert et al. (2003) for an example) or
immediately after it has been extinguished (as is the case
when patients are allowed to look towards the blind field
location they believe a target was presented in Weiskrantz
et al. (1974)). The fact that introducing a delay between
blind field target presentation and action initiation eliminated any statistical relationship between grip scaling and
target size in one hemianopic patient, suggests that actionblindsight does rely on the immediate initiation of actions
towards blind field targets to be successful (Rossetti, 1998).
2.3. ‘Action-blindsight’ and the automatic pilot
So far we have suggested that action-blindsight depends
on the integrity of visual pathways that terminate in
7
It is important to note that some influence of the illusion on grasping can
be seen in these studies although the magnitude of the effect is far smaller
than the influence observed on perception (Westwood et al., 2000). In
addition, recent work has demonstrated that the immunity of grasping
actions to illusory contexts is evident throughout the course of a movement,
suggesting that the programming of the movement, and not on-line control,
is responsible for the fact that actions are impervious to illusions (Danckert
et al., 2002). This contention is far from uncontroversial (Glover and Dixon,
2001). What we are intending to suggest here is not a distinction between
planning and on-line control but a distinction between the immediate and
delayed control of actions.
1042
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
the PPC (i.e. the dorsal visual stream) and that rely upon
immediate initiation of actions in response to blind field
stimuli (see Rossetti (1998) for review). Given that these
residual abilities are carried out by definition in the
absence of visual awareness of the targets, one further
suggestion would imply that action-blindsight operates in
an automatic manner. Indeed, recent evidence from
healthy individuals and other neurological disorders does
imply that the PPC often functions automatically, rapidly
modifying visually guided hand movements often in
contradiction to conscious commands (Pisella et al.,
2000). Some of the evidence for automatic processing in
the PPC will be reviewed here (see also Rossetti and
Pisella (2002), Pisella and Rossetti (2000) and Rossetti
et al. (in press)) before we discuss the implications of this
work for action-blindsight.
As mentioned above, recent research in patients with a
neurological disorder known as optic ataxia suggests that
the dorsal ‘action’ pathway often operates in a largely
automatic manner (Milner and Dijkerman, in press). Optic
ataxia is an impairment observed following lesions of
superior parietal cortex, often bilaterally (Jeannerod and
Rossetti, 1993; Perenin and Vighetto, 1988; De Renzi, 1974,
1982; Vighetto and Perenin, 1981). Although no motor or
visual sensory deficits are typically observed on clinical
testing, closer examination shows that the patient has great
difficulty directing their arm towards a visual target
presented in their peripheral visual field (Perenin and
Vighetto, 1988; Vighetto and Perenin, 1981). Typically, an
interaction is found between the hand used to carry out the
action and the visual field in which the action is directed,
such that the patient’s performance is worse with the hand
contralateral to the lesion when (s)he reaches into the
contralateral peripheral visual field, whereas the deficit is
minimal when the ipsilateral hand reaches into the
ipsilateral field. In addition, these impairments are most
evident for movements made in immediate response to the
appearance of a visual target.
Recent work has recast the impairments observed in optic
ataxia as a disruption to what has been dubbed a ‘parietal
automatic pilot’ (Pisella et al., 2000). Primary evidence for
this account of optic ataxia comes from the double-step
pointing task (Prablanc et al., 1986). In this paradigm
subjects are required to point to targets that on a small
percentage of trials can be perturbed after movement onset.
In healthy individuals, pointing movements can be corrected
‘on-line’ to such perturbations in location or even size of the
target object (Rossetti and Pisella, 2002; Pisella and Rossetti,
2000; Prablanc et al., 1986; Desmurget et al., 1995; Goodale
et al., 1986; Gréa et al., 2000; Pélisson et al., 1986; Prablanc
and Martin, 1992; Rossetti et al., 2000). That is, subjects are
able to make rapid adjustments to goal-directed actions when
some aspect of the target (e.g. location or size) is perturbed
(see Rossetti and Pisella (2002) and Rossetti et al. (2000)) for
review). In addition, after a fast pointing movement has been
programmed and initiated toward a visual target, it can be
corrected without a significant increase in movement time
(Goodale et al., 1986; Pélisson et al., 1986; Prablanc and
Martin, 1992). That is, the rapid adjustment of the movement
to the perturbed target location occurs without the need to reprogram a new motor output. Finally, such on-line corrections can be observed whether or not the target displacement
is consciously perceived (Goodale et al., 1986; Pélisson et al.,
1986; Prablanc and Martin, 1992). These results suggest that
such corrections are executed automatically.
Neuroimaging evidence has revealed increased activation in a network of structures including the PPC when
such automatic corrections to pointing movements are made
(Desmurget et al., 2001). In addition, when functioning in
the PPC is disrupted due to transcranial magnetic stimulation (TMS), the ability to correct movements to target
perturbations is also disrupted (Desmurget et al., 1999). This
evidence strongly implicates the PPC in the on-line,
automatic control of visually guided actions. In light of
this research, the impairments characteristic of optic ataxia
can be reconsidered as an impairment of real-time control of
visually guided actions rather than of motor programming
(see Rossetti and Pisella (2002) for review). It may be the
case that the same areas implicated in the on-line control of
movements discussed above are also responsible for actionblindsight. In at least one neuroimaging study of a blindsight
patient activity in dorsal extrastriate regions that project to
the PPC was observed (Baseler et al., 1999). Further
neuroimaging work that explicitly examines behaviours
such as pointing or saccading to blind field targets and not
simply passive neural responses to blind field stimuli, will
be needed to determine the veracity of the claim that actionblindsight depends on processing in the PPC.
If the ability to correct rapid goal-directed actions can
bypass conscious awareness, to what extent can such an
automatic system process visual information? A modification of the double-step pointing paradigm was used to
explore this question (Rossetti and Pisella, 2002; Pisella and
Rossetti, 2000; Pisella et al., 1998, 1999). In this version of
the paradigm target perturbations could be used as a
go-signal to perform an in-flight correction to acquire the
new target location (the ‘location-go’ task) or alternatively,
as a stop-signal (the ‘location-stop’ task) to interrupt the ongoing movement. Therefore, the two types of response, go
or stop, required alteration to an already planned (and
presumably ongoing) pointing action. For both versions of
the task subjects were instructed to initiate a rapid pointing
movement towards the target. Movement duration was
tightly controlled using auditory feedback so that a sample
of movement times was taken (i.e. if the subject moved too
slowly a tone sounded to inform them that a quicker
movement was required). Successful performance in the
‘location-stop’ task would presumably lead to a cessation of
the rapid pointing movement. Initially, it was expected that
any failure to comply with task instructions would lead to a
movement that was completed to the original target
location—in other words an inability to alter the first
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
motor program made towards the initial target location
(Pisella et al., 2000). In striking contrast to this prediction, a
significant percentage of corrective movements were
performed in the direction of the target jump in spite of
the instruction to halt their movements. These corrections
were considered to be automatic because they were
produced spontaneously by naive subjects against their
own intention to stop their movement in accordance with
instructions. After touching the displaced target, subjects
were fully aware of their mistakes and impulsively
expressed frustration at their ‘error’. This ‘automatic pilot’
(see also Place (2000)) systematically activated during
movement execution led subjects to produce ‘disallowed’
corrective movements over a narrow range of movement
times (between 150 and 300 ms). Importantly, the same rate
of movement corrections observed in the location-stop
condition were also found in the control ‘location-go’
condition where subjects were allowed to adjust their
pointing movement in response to target perturbations. That
is, whether they were asked to adjust or stop their pointing
movements in response to target perturbations, subjects
made approximately the same number of corrections. Only
movements slower than 300 ms could be fully controlled by
voluntary processes (Pisella et al., 2000).
In contrast to the performance of healthy individuals on
the location-stop task, a patient with a bilateral lesion of
the PPC (patient IG) showed a complete lack of on-line
automatic corrective processes, whereas the slower
intentional motor processes were preserved (Pisella et
al., 2000). That is, when asked to interrupt her rapid
pointing movements to target perturbations IG was fully
able to do so, unlike healthy controls, suggestive of a
disruption to her automatic pilot (the same pattern of
behaviour has been observed in another bilateral optic
ataxia patient (Pisella, personal communication). This
result suggests that rapid pointing movements are
controlled by a posterior parietal ‘automatic pilot’ located
in the dorsal stream. In contrast, slow movements are
controlled by intentional motor processes that do not
necessarily rely as heavily on the posterior parietal cortex.
Thus the notion of an automatic pilot extended that of
‘hand-sight’ (Rossetti et al., 2000) in the sense that it
refers not only to unconscious visual processing by the
action system, but also to an autonomous use of visual
information which bypasses and even counteracts intentional control. For the purposes of the current paper we
are suggesting that the parietal automatic pilot may also
be the final point in the neural pathway that is responsible
for action-blindsight.
3. Conclusion: action-blindsight—the automatic pilot
in slow motion?
We have previously demonstrated that a greater
degree of sparing of the PPC is associated with more robust
1043
action-blindsight (Danckert et al., 2003). In those same
patients we attempted to explore the possibility that
automatic corrections of pointing movements would also
be possible even though the patients were never aware of the
presence of the targets or perturbations in target locations
(Danckert and Rossetti, unpublished data). That is, if actionblindsight does indeed depend on the integrity of a residual
pathway that terminates in the PPC—the same pathway we
suggest is responsible for automatic corrections of pointing
movements to target perturbations—then similar corrections should be evident in action-blindsight patients for
target perturbations occurring in the blind field. We found
no such evidence for an ability to correct movements to
blind field target perturbations (Danckert and Rossetti,
unpublished data; Fig. 3).
The absence of significant adjustments to target perturbations in the blind field could be due to several factors that
we raise here for potential future studies. Perhaps the most
striking factor involved is movement duration. The movement durations of both patients for perturbed trials were
generally longer than around 400 ms—outside the range of
automatic corrections (or involuntary errors) seen in healthy
individuals (Pisella et al., 2000). This is an important point.
When asked to adjust their rapid pointing movements to
perturbations in target location, healthy individuals were
only able to do so on approximately 15% of trials, all at
movement durations of between 150 and 300 ms (Pisella
et al., 2000). The evidence to suggest that these were
‘automatic’ corrections comes from the observation that a
similar percentage of movement corrections were observed
even when subjects were told to stop their movement in
response to a location perturbation—once again, all
occurring at movement durations of around 300 ms or less
(Pisella et al., 2000). This time frame is quite a bit shorter
than the average movement duration seen in either of our
hemianopic patients (for JR mean MDZ540.2 ms; for YP
mean MDZ634.24 ms). What implications does this have
for the suggestion that the secondary visual pathway from
the colliculus to the PPC is responsible both for ‘actionblindsight’ and the automatic pilot? The first, most obvious
explanation would suggest that both behaviours (actionblindsight and the parietal automatic pilot) are not supported
by the same pathway. Second, the automatic pilot (V1
intact) requires a heavier visual input than is required for
action-blindsight. In other words, in order to show
corrections to rapid pointing movements the PPC may
require input from V1. Alternatively, the same neural
pathway may be involved but for patients with blindsight
this pathway may operate in a different manner. The
suggestion here is that to localize blind field targets or to
adjust a pointing movement to a target perturbation, the
same pathway from the colliculus to the PPC via the
pulvinar is involved. But for action-blindsight patients
the uncertainty induced by the conscious awareness of their
field defect makes this pathway function more slowly than
would otherwise be the case—the automatic pilot operating
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
A
fixation LED
targets
B
300
end x-position
1044
250
200
150
Patient JR
100
1
2
3
4
5
target
starting position
end x-position
450
touch screen
monitor
400
350
300
Patient YP
250
perturbed target trial
1
C
end x-position
fixation
auditory tone
target 1
3
4
5
target
300
250
200
150
Patient JR
100
movement
backward
(3 to 2)
target 3
forward
(3 to 4)
450
2 secs
1 2 3 4 5
forward perturbation
end x-position
target 2
1 2 3 4 5
backward perturbation
2
400
350
300
Patient YP
250
backward
(3 to 2)
target 3
forward
(3 to 4)
Fig. 3. Panel A. Schematic representation of the experimental setup examining pointing behaviour in two blindsight patients. The patient started by resting their
finger on a starting position at the bottom of a touch screen monitor. The patient fixated a constantly illuminated LED taped to the far side of the monitor. For
unperturbed trials an auditory tone was presented coincident with the onset of the target which remained on the screen for a period of 2 s. Perturbed trials
always began with a target at the central location (location 3 in the schematic). For perturbed trials (50% of all trials) the location of the initial target moved
either to the right (termed a forward perturbation) or the left (termed a backward perturbation) initiated by movement onset (i.e. when the patient lifted their
finger from the touch screen). Panel B. Mean end point along the x-axis for patient JR (above) and YP (below) for unperturbed targets. Patient JR’s movements
were significantly correlated with target location while YP’s were not (but see Danckert et al. (2003) for a different version of this task in which YP does show
some degree of action blindsight). Panel C. Mean end point along the x-axis for pointing movements to perturbed targets for JR (above) and YP (below).
Neither patients’ pointing movements showed any significant relationship to the perturbed target locations. In both panels B and C the dotted lines represent
linear regression lines fitted to the patients’ data.
in slow motion. This hypothesis can be easily tested simply
by forcing patients with hemianopic field defects to point to
blind field targets within tightly controlled time frames (less
than 300 ms). While one may not expect blindsight patients
to perform at the same level as controls, the hypothesis
proposed here would suggest that performance for both
static and perturbed blind field targets would improve
relative to performance at longer time frames. Although
both of our blindsight patients tended to have long
movement durations, JR’s movements were on average
faster than YP’s. Given that the ability to localize
unperturbed blind field targets was more robust for JR
than it was for YP (Danckert et al., 2003), this provides
some support for the notion that fast, automatic control of
movements is required for hemianopic patients to demonstrate action-blindsight.
The present comparison between action-blindsight and
optic ataxia suggests that at least two types of afferences to
the PPC may participate in the control of action. The dorsal
‘action’ pathway from V1 through to the PPC and the more
limited subcortico-cortical pathway from the colliculus to the
PPC via the pulvinar. While it may be the case that this more
minor subcortico-cortical pathway cannot enable ‘normal’
visuo-motor behaviour (see the comparison between visual
agnosia and blindsight in Rossetti and Pisella (2002)), it is
nevertheless true that it supports some control of skilled
actions. Importantly, this control is likely to be automatic in
nature (Rossetti and Pisella, 2003). The main challenge
arising from the present result is to delineate the contribution
of these two pathways, as well as other possible pathways, to
the integrated control of visually guided actions both in
healthy individuals and in patient populations.
J. Danckert, Y. Rossetti / Neuroscience and Biobehavioral Reviews 29 (2005) 1035–1046
Acknowledgements
The authors wish to thank Claude Prablanc, Denis
Pélisson, Laure Pisella, Gilles Rode, Alain Vighetto,
Hisaaki Ota, Aarlenne Khan and Masami Ishihara for
numerous fruitful discussions. This work was supported by
funds from the McDonnel-Pew foundation (YR), from Lyon
University (JD), from the Leverhulme International
Research Exchange Trust (JD and YR), from Programme
Hospitalier de Recherche CLinique (PHRC 30251 to YR)
and from the Natural Sciences and Engineering Research
Council of Canada (Discovery and Canada Research Chair
grants to JD).
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